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  • Title: [Hormonal control of the metabolism of collagen].
    Author: Borel JP, Maquart FX, Randoux A.
    Journal: Pathol Biol (Paris); 1984 Sep; 32(7):795-812. PubMed ID: 6387598.
    Abstract:
    This paper summarizes the results of hormonal studies applying to collagen metabolism that were published during the last 10 years. This general review demonstrates that most of the hormones, when they act on this metabolism, either decrease the amount of synthesized collagen or increase its catabolism. This effect is demonstrated on whole living animals, in isolated organs, in pathological cases such as corticosteroid induced osteoporosis, and more directly in cell cultures. At physiological levels, some of the effects may be slight or biphasic but at pharmacological levels glucocorticoids and estrogens are strongly inhibiting. These inhibiting effects may be ascribed to various stages of collagen biosynthesis: transcription of the genes, translation of mRNA, post-translational reactions, that are particularly developed in the case of collagen and particularly sensitive to the hormone action. Intracellular degradation of collagen represents an important way of control for this biosynthesis and is noticeably activated by the system of cAMP and some prostaglandins. Finally, collagenases acting on the extracellular fibrils are stimulated by several groups of hormones such as thyroid hormone, testosterone, parathyroid hormone. This increase in catabolism acts in the sense of a fast decrease in the amount of collagen, confirming that most of the hormonal systems are aimed at decreasing both the synthesis of new collagen and the number of mature fibers existing in a given connective tissue. On the other hand, many growth factors and several hormones such as insulin and somatomedins are able to activate the mitoses in the cells that are know to produce collagen, and for this reason, indirectly stimulate the synthesis of this fibrous protein. It is of interest to point out that every time the organism needs depositing more collagen in any zone of the extracellular matrix, it has to send mobile cells from other tissues or to activate the divisions of the cells already present in the concerned tissue. This process is particularly conspicuous in the case of inflamed tissues. It is proposed as a general rule that decreases in the collagen amounts may be triggered by very fast hormonal mechanisms acting both to stop biosynthesis and to activate degradation, whereas the increase in collagen layering depends on indirect and slow mechanisms in which cell divisions represent the first event.
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